Ultraviolet light induces reactivation in a murine model of cutaneous herpes simplex virus-1 infection

We have developed a model of cutaneous herpes simplex virus-1 (HSV-1) react ivation in SKH-1 hairless mice which closely mimics the condition in humans . Sixty plaque-forming units of HSV-I strain 17 syn+ were applied to a supe rficially abraded area on the Lateral body wail. More than 85% of mice deve loped primary HSV-1 infection characterized by a zosteriform pattern of cut aneous vesiculation and ulceration. Approximately one-third of mice with pr imary skin lesions succumbed to neurologic disease and in the remaining mic e cutaneous lesions healed completely. Subsequent exposure of healed areas to two minimal inflammatory doses of UV resulted in recrudescence of skin l esions in the irradiated areas in almost 60% of mire. Lesions appeared appr oximately 4 days after irradiation, persisted for 3-5 days and then resolve d completely. Reactivation rarely resulted in death due to neurologic disea se, Primary lesions had a histologic appearance typical of cutaneous HSV-1 infection with vesicles and focal epithelial necrosis accompanied by the fo rmation of epithelial syncytial cells and the presence of herpetic intranuc lear inclusion bodies. In primary lesions HSV-I was demonstrated by immunoh istochemistry, polymerase chain reaction and culture. In reactivated lesion s epithelial syncytia and inclusion bodies were not seen; however, virus wa s demonstrable by polymerase chain reaction and culture. Exposure of the un infected side to UV did not stimulate disease recurrence suggesting that lo cal effects of UV rather than systemic immunosuppression were responsible f or reactivation. Reactivation could also be obtained with two minimal infla mmatory doses of UV from a UV-340 light source which emits light approximat ing the solar spectrum.